Strains carrying deletions in both the SSA1 and SSA2 HSP70 genes of Saccharomyces cerevisiae exhibit pleiotropic phenotypes, including the inability to grow at 37 degrees C or higher, reduced growth rate at permissive temperatures, increased HSP gene expression, and constitutive thermotolerance. A screen for extragenic suppressors of the ssa1 ssa2 slow-growth phenotype identified a spontaneous dominant suppressor mutation, EXA3-1 (R.J. Nelson, M. Heschl, and E.A. Craig, Genetics 131:277-285, 1992). Here we report that EXA3-1 is an allele of HSF1, which encodes the heat shock transcription factor (HSF). Strains containing the EXA3-1 allele in a wild-type background exhibit a 10- to 15-fold reduction in HSF activity during steady-state growth conditions as well as a delay in the accumulation of the SSA4, HSP26, and HSP104 mRNAs after a heat shock. EXA3-1-mediated suppression is the result of a single amino acid substitution of a highly conserved residue in the HSF DNA-binding domain which drastically reduces the ability of HSF to bind to heat shock elements as evaluated by band shift analysis. Together, these results indicate that the poor growth of ssa1 ssa2 strains is the result, at least in part, of the overproduction of a deleterious heat shock protein(s). This conclusion is supported by the fact that the levels of at least some heat shock proteins are reduced in ssa1 ssa2 cells containing the EXA3-1 allele. Surprisingly, strains containing the EXA3-1 allele in a wild-type HSP70 background grow early as well as the wild-type strain over a wide temperature range, displaying only a slight reduction in growth rate at 37 degrees Celsius, indicating that cells contain significantly more HSF activity than is require for growth under steady-state conditions.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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